Low muscle mass and chronic lung disease are common among people with HIV (PWH), but whether low muscle mass is associated with a faster decline in lung function in this population remains unknown. We aimed to determine the prevalence and associated factors of low muscle mass, and the association between low muscle mass and lung function decline in PWH.

A prospective study on PWH from the Copenhagen Comorbidity in HIV Infection (COCOMO) study.

Skeletal muscle index (SMI) was assessed with computed tomography and low muscle mass was defined as SMI below the lowest 5% of a healthy population. Lung function was measured as forced expiratory volume in 1 s (FEV 1 ) at baseline and 2-year follow-up. We used logistic regression to investigate potential risk factors for low muscle mass. Using linear mixed models, we investigated if low muscle mass was associated with a faster FEV 1 decline.

We included 509 PWH, and 16% had low muscle mass. Older age, male sex, lower BMI, and high concentrations of interleukin 6 and tumor necrosis factor alpha were associated with low muscle mass. Low muscle mass was not associated with a faster FEV 1 decline (35.9 versus 34.0 ml/year in PWH with and without low muscle mass, respectively; P  = 0.69).

Almost one in six PWH had low muscle mass, mirroring the general population. Traditional risk factors and inflammatory markers were associated with low muscle mass. We found no association between low muscle mass and a faster FEV 1 decline among PWH.

This study investigates the associations between volatile organic compound (VOC) exposure and sarcopenia, focusing on independent and combined effects and exploring potential biological mechanisms. Utilizing data from the National Health and Nutrition Examination Survey, we applied logistic regression to examine associations between individual VOCs and sarcopenia, while restricted cubic splines (RCS) assessed dose-response relationships. Weighted quantile sum (WQS) and Bayesian kernel machine regression (BKMR) evaluated mixed exposure effects. Mediation analyses explored the roles of potential mediators, alongside bioinformatic analyses to investigate the underlying mechanisms. Multivariable logistic regression identified significant associations between specific VOCs and sarcopenia, particularly for DHBMA (OR=2.71, 95 % CI: 1.62-4.55). RCS confirmed both linear and nonlinear associations of specific VOCs. WQS analysis corroborated a synergistic effect of mixed VOC exposures and increased sarcopenia risk (OR=1.64, 95 % CI: 1.14-2.36), and BKMR analysis further confirmed this positive relationship. Mediation analysis revealed that inflammation, oxidative stress, and renal function partially mediated these associations (mediated proportions: 4.67-11.00 %). Bioinformatic analyses highlighted apoptosis-related targets and pathways as key mechanisms underlying the observed associations. This study provides comprehensive evidence linking VOC exposure to sarcopenia, emphasizing the importance of reducing VOC exposure to prevent sarcopenia and associated health risks.

Sarcopenia is a clinicopathological condition characterized by a decrease in muscle strength and muscle mass, playing a crucial role in the prognosis of cancer. Therefore, this study aims to investigate the association between sarcopenia and both all-cause mortality and cancer-specific mortality among cancer patients. Furthermore, we plan to develop risk prediction models using machine learning algorithms to predict 3-year and 5-year survival rates in cancer patients.

This study included 1095 cancer patients from the National Health and Nutrition Examination Survey (NHANES) cohorts spanning 1999-2006 and 2011-2014. Initially, we used the Least Absolute Shrinkage and Selection Operator (LASSO)-Cox regression models for feature selection. Subsequently, we employed multivariable Cox regression models to investigate the association between sarcopenia and all-cause and cancer-specific mortality in cancer patients. We developed five machine learning algorithms, including Support Vector Machine (SVM), Logistic Regression (LR), Random Forest (RF), LightGBM, and XGBoost, to predict 3-year and 5-year survival rates and to perform risk stratification.

The multivariable COX regression model showed sarcopenia significantly increases the risk of all-cause mortality (HR = 1.33, 95%CI:1.05, 1.70, P = 0.0194) and cancer-specific mortality (HR = 1.67, 95%CI:1.09, 2.55, P = 0.0176) in cancer patients. Among the five machine learning algorithms developed, the LightGBM model demonstrated strong performance in the 3-year and 5-year survival prediction tasks, making it the optimal model selection. Decision curve analysis and Kaplan-Meier curves further confirmed our model's ability to identify high-risk individuals effectively.

Sarcopenia significantly increases the risk of mortality in cancer patients. We developed a survival prediction model for cancer patients that effectively identifies high-risk individuals, thereby providing a foundation for personalized survival assessment.

Age-related muscle function decline is a major impediment to healthy ageing. We aimed to investigate the association between a panel of Alzheimer's disease-related biomarkers and longitudinal trajectories of muscle strength, while exploring the influence of cognitive function.

In this cohort study, we gathered data from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K), an ongoing prospective study that includes adults aged 60 years and older, from central Stockholm, Sweden. We included data from baseline to the fourth follow-up (March 21, 2001, to Dec 31, 2016). Seven Alzheimer's disease-related blood biomarkers were measured in dementia-free, community dwelling participants: total tau, phosphorylated tau181 (p-tau181), phosphorylated tau217 (p-tau217), amyloid β 40 and 42, neurofilament light chain, and glial fibrillary acidic protein (GFAP). Muscle strength was measured through the handgrip strength and chair-stand tests. Linear mixed models were used to explore the association between baseline Alzheimer's disease-related biomarkers and muscle strength trajectories.

The baseline SNAC-K cohort included 3363 individuals, of whom 1953 participants were included in our analyses (mean age 70·2 [SD 9·1] years; 780 [39·9%] male and 1173 [60·1%] female participants). In adjusted models, higher concentrations of p-tau181 (β per year 0·93 [95% CI 0·71 to 1·16]; p<0·0001), p-tau217 (β per year 1·31 [1·03 to 1·58]; p<0·0001), neurofilament light chain (β per year 0·76 [0·56 to 0·96]; p<0·0001), and GFAP (β per year 0·37 [0·21 to 0·53]; p<0·0001) were associated with an accelerated decline of chair-stand performance over time. The adjustment for Mini-Mental State Examination (MMSE) score led to the attenuation of these associations. Higher concentrations of p-tau181 (β per year -0·12 [95% CI -0·17 to -0·07]; p<0·0001), p-tau217 (β per year -0·13 [-0·20 to -0·07]; p<0·0001), and neurofilament light chain (β per year -0·05 [-0·09 to -0·001]; p=0·047) were also associated with faster handgrip strength decline, with no attenuation after adjusting for MMSE score. Sex-specific differences were observed, with female participants showing a stronger association between biomarker concentrations and muscle strength decline than male participants, particularly in the chair-stand test.

Our findings suggest that blood Alzheimer's disease-related biomarkers might help estimate progressive muscle strength decline among older adults, elucidating the influence of brain pathology and cognitive ageing on this association. These Alzheimer's disease-related biomarkers could aid in identifying individuals for early intervention to prevent sarcopenia.

The Swedish Research Council, the Swedish Ministry of Health and Social Affairs, and the County Councils and Municipalities.

This study aimed to examine the association between relative handgrip strength (rHGS) and nonalcoholic fatty liver disease (NAFLD) incidence, considering abdominal obesity (ABO) status. This nationwide Korean cohort included 24,297 participants without NAFLD at baseline. Participants were categorized into sex-specific tertiles of rHGS (low, mid, and high). Multivariate Cox proportional hazards regression models were used to evaluate NAFLD incidence in relation to rHGS levels and/or ABO status. Over 100,381 person-years of follow-up, 1,735 participants (10.81% men and 6.01% women) developed NAFLD. High rHGS was associated with a 29% and 60% risk reduction for incident NAFLD in men and women, respectively, compared with low rHGS, despite men having significantly higher rHGS than women. Conversely, ABO increased NAFLD risk by 2.3 and 3.8 times in men and women, respectively. Even among women with ABO, mid and high rHGS were associated with a 23% and 36% risk reduction in incident NAFLD, respectively, compared with low rHGS. However, there was no significant relationship between rHGS levels and NAFLD incidence in men with ABO. Higher rHGS levels may prevent NAFLD, particularly in women. In individuals with ABO, high rHGS markedly decreased NAFLD risk in women but not in men.

Sarcopenic obesity is characterized by a combination of obesity and sarcopenia. Body round index (BRI) is a novel anthropometric index that can more accurately assess body and visceral fat levels than body mass index or waist circumference. This study used data from the National Health and Nutrition Examination Survey (NHANES) to explore the relationship between BRI and handgrip strength (HGS) and muscle quality index (MQI) in American adults aged 20 and over.

This study used cross-sectional data from the 2011-2014 National Health and Nutrition Examination Survey (NHANES) with complete data on BRI, HGS, and MQI. We used multivariate linear regression models and smooth curve fitting methods to explore the relationship between BRI and HGS and MQI. In addition, subgroup analyses and interaction tests were performed to further analyze the potential association between these variables.

A total of 5466 participants were finally included in this study, of whom 2807 were males and 2659 were females. The results showed that BRI was positively correlated with HGS and negatively correlated with MQI. In the fully adjusted model, the negative correlation between BRI and MQI was (β= -0.08, 95% CI = -0.08, -0.07), while the positive correlation with HGS was (β= 0.3 8, 95% CI = 0.29, 0.46), indicating that for every unit increase in BRI, MQI decreases by 0.08 units and HGS increases by 0.38 units (P < 0.0001). In addition, the relationship between BRI and HGS is an L-shaped curve. An inflection point is determined when BRI reaches 3.42. Before this threshold, for every unit increase in BRI, HGS increases significantly (β = 2.19, 95% CI = 1.66, 2.72).

The results showed that BRI was positively correlated with HGS and negatively correlated with MQI, meaning that higher BRI was associated with higher HGS and lower MQI. This highlights the importance of body fat distribution in muscle health and suggests that BRI can be used as an effective anthropometric indicator to predict grip strength and muscle mass.

There is limited evidence on a longitudinal association between an anti-inflammatory diet (AID2) and low muscle mass (LMM3) in older adults. This study used data from the 2011-2017 Chinese Longitudinal Survey of Health and Longevity (CLHLS) to analyze the association between AID and LMM risk using cox regression models. At the same time, restricted cubic spline analysis and subgroup analysis were carried out. The study involved 675 elderly people in China. The incidence of low muscle mass was 34.67 %. The anti-inflammatory diet had a significant protective effect on muscle mass in older adults (HR = 0.82, 95 % CI: 0.70-0.96). In addition, the LMM risk was 32 % lower in the high AID rating group (T2) compared to the low AID rating group (T1). We encourage older adults to improve muscle mass by increasing their anti-inflammatory dietary intake to prevent or delay the onset of sarcopenia.

Skeletal muscle mass is a critical prognostic factor across various cancers; however, its differential impact on survival outcomes and the nature of postoperative changes remains inadequately explored. This study investigates the influence of preoperative skeletal muscle mass on survival and postoperative trends in skeletal muscle mass across gastrointestinal cancer types.

The total psoas major muscle volume (TPV) was utilized as a skeletal muscle index, obtained from CT images of patients with gastrointestinal cancer. TPV measurements were extracted at multiple time points to assess changes over time.

A total of 1798 patients were included (esophageal: 554; gastric: 539; colorectal: 705). Patients with low skeletal muscle mass exhibited poorer prognoses across all cancer types. Among these, 969 patients (esophageal: 307; gastric: 278; colorectal: 384) had available postoperative follow-up CT scans at 1, 2, and 3 years. Annual decreases in TPV were observed across all cancer types; however, patients with colorectal cancer demonstrated a smaller decline in skeletal muscle mass compared to those with esophageal and gastric cancers (p < 0.05). In gastric and esophageal cancer patients, TPV was significantly lower in those with recurrence. Additionally, in gastric cancer, the reduction in TPV after distal gastrectomy was less than that observed after proximal or total gastrectomy.

This study underscores the prognostic significance of skeletal muscle mass in gastrointestinal cancer and its dynamic postoperative changes, highlighting the need for further investigation to enhance patient outcomes as the global cancer burden increases.

The relationship between BMI and chronic kidney disease is controversial, likely due to the inability of BMI to accurately define body composition and adipose tissue distribution. Our objective was to evaluate the synergistic contribution of fat-free mass, fat mass, visceral (VAT) and subcutaneous (SAT) adipose tissue, to glomerular filtration rate (GFR) in a large cohort of subjects.

A cross-sectional study of 9704 subjects (72% female, median age 47y, median BMI 28.1 kg/m2) was carried out. Each patient underwent an anthropometric assessment (weight, height, waist circumference, % of body fat by body skinfolds), an ultrasound measurement of VAT and SAT and blood sampling to measure metabolic syndrome (MS) parameters and serum creatinine. GFR was estimated using the EPI-CKD equation. MS was defined according to the harmonized criteria.

Among 9,704 subjects, 61.1% had a normal renal function, while 29.3% reported a reduction, from slightly to severely. The BMI was initially negatively associated with GFR in the univariate model (β = -0.32, 95% CI: -0.39, -0.25), but after adjusting for %body fat, the association was lost. We then split the BMI into its two components, Fat Mass Index (FMI) and Fat Free Mass Index (FFMI), and observed that FMI (β = -1.23, 95% CI: -1.35, -1.12) and FFMI (β = 0.79, 95% CI: 0.65, 0.92) were associated with a decrease and an increase in GFR, respectively. VAT (β = -1.83, 95% CI: -2.00, -1.67) and SAT (β = 3.21, 95% CI: 2.86, 3.57) were independently associated with a decrease and an increase in GFR, respectively. Similar results were obtained when studying the association between BMI, body composition, adipose tissue distribution, and the risk of reduced GFR (<90 ml/min/1.73 m2). Stratification by sex and MS did not substantially alter the results. A significant association between VAT and reduced GFR was observed only in women.

Our study highlights the importance of considering body composition and fat distribution when assessing renal function.

Frailty, characterized by functional decline and disability, is an emerging public health concern in aging populations. Chronic inflammation and low high-density lipoprotein cholesterol (HDL-C) levels are key contributors to the progression of frailty. This study aims to examine the association between the ratio of high-sensitivity C-reactive protein (hs-CRP) to HDL-C and frailty among middle-aged and older adults in the United States.

Our study included participants aged 45 years and older from the 2015-2020 National Health and Nutrition Examination Survey (NHANES). Logistic regression and restricted cubic spline (RCS) analysis were utilized to assess the relationship between the hs-CRP/HDL-C ratio and frailty, adjusting for potential confounding covariates. Mediation analysis was performed to determine whether plasma proteins mediated this association. Least absolute shrinkage and selection operator (LASSO) regression was employed to identify variables strongly correlated with frailty, and a nomogram was subsequently developed based on these variables.

Our study included 3,626 middle-aged and older participants, among whom 787(21.7%) were identified as frailty. After adjusting for all covariates, a high hs-CRP/HDL-C ratio was identified as a significant risk factor for frailty (OR = 1.736, 95% CI: 1.009-2.988). RCS analysis disclosed a nonlinear correlation between the hs-CRP/HDL-C ratio and frailty incidence. Furthermore, mediation analysis suggested that albumin and globulin partially mediated this association, accounting for 37.82% and 11.23% of the indirect effect, respectively. A nomogram, constructed using variables selected via LASSO regression, exhibited promising discriminative ability, with an area under the curve (AUC) of 79.7% (95% CI: 77.7-81.75%).

Our findings suggest that a higher hs-CRP/HDL-C ratio is associated with an increased risk of frailty among middle-aged and older adults. Albumin and globulin partially mediate this relationship. Additionally, the nomogram developed in our study shows strong predictive ability for identifying individuals at high risk of frailty in this population.

To investigate the associations between periodontal inflammation-as determined by the periodontal inflamed surface area (PISA)-and serum inflammatory markers in community-dwelling older adults in Japan.

This cross-sectional study included 470 adults (mean age: 73.1 years). The composite inflammatory marker z-score (CIMZ) was calculated as the sum of the participants' individual z-scores for C-reactive protein (CRP), interleukin-1beta (IL-1β), IL-6 and tumour necrosis factor-α (TNF-α). The associations of PISA (quartiles) with individual biomarkers (continuous, log-transformed) and CIMZ (dichotomized, highest quartile or not) were assessed using linear or Poisson regression models.

Compared with participants in the lowest PISA quartile (Q1), those in Q3 and Q4 had significantly (p < 0.05) higher CRP and IL-6 levels. Statistically significant linear trends (ptrend < 0.05) across the PISA quartiles were observed for CRP and IL-6. The multivariable adjusted prevalence ratios (95% confidence intervals) of high CIMZ (reference: Q1) were 1.20 (0.68-2.14), 1.66 (0.96-2.88) and 1.90 (1.08-3.34) (ptrend = 0.01) in individuals in PISA Q2-Q4.

Older adults with high periodontal inflammation had high serum CRP and IL-6 concentrations and composite summary inflammatory indicator values. Periodontal inflammation is a potential modifiable factor of elevated inflammatory status among older adults in Japan.

The relationships between grip strength asymmetry and cardiovascular, respiratory, and cancer outcomes and all-cause mortality remain unclear.

Among 443,132 UK Biobank participants enrolled from 2006 to 2010, grip strength asymmetry was defined as the ratio of left-hand grip strength (kg) to right-hand grip strength (kg) <0.9 or >1.1. The Cox proportional model was employed to assess the associations of grip strength asymmetry with cardiovascular, respiratory, and cancer outcomes and all-cause mortality. Net reclassification improvement was assessed to evaluate the improvement in risk discrimination for outcomes after adding grip strength asymmetry to the model with established office-based risk factors.

After a mean follow-up of 12.1 years, 28,478 (6.4%) deaths occurred. grip strength asymmetry was significantly associated with all-cause (hazard ratio: 1.096; 95% CI=1.070, 1.122), cardiovascular disease (hazard ratio: 1.141; 95% CI=1.071, 1.216), respiratory disease (hazard ratio: 1.183; 95% CI=1.076, 1.301), chronic obstructive pulmonary disease (hazard ratio: 1.284; 95% CI=1.087, 1.516), and cancer (hazard ratio: 1.051; 95% CI=1.017, 1.086) mortality. Significant associations of grip strength asymmetry with cardiovascular disease (hazard ratio: 1.029; 95% CI=1.004, 1.054), respiratory disease (hazard ratio: 1.074; 95% CI=1.051, 1.103), chronic obstructive pulmonary disease (hazard ratio: 1.123; 95% CI=1.038, 1.215), and colorectal cancer (hazard ratio: 1.051; 95% CI=1.037, 1.066) incidence were observed. Moreover, adding grip strength asymmetry to a model with established office-based risk factors significantly improved the ability to predict all-cause, cardiovascular disease, and respiratory disease mortality.

Grip strength asymmetry was associated with a range of adverse health outcomes and may have clinical use in predicting all-cause, cardiovascular disease, and respiratory disease mortalities. Further studies are warranted to validate the clinical value of the grip strength asymmetry assessment.

The aim of this study was to evaluate the accuracy of screening tools for sarcopenia and to determine whether the same or different cutoff points should be applied in patients with chronic stroke.

Sixty-eight participants with residual hemiparetic deficit for over 6 months were enrolled. We evaluated the accuracy of calf circumference, SARC-F questionnaire, SARC-CalF, and Ishii's score chart using the Asia Working Group for Sarcopenia (AWGS) 2019 revised criteria as the gold standard.

Sarcopenia was identified in 22 participants (32.4%) based on the AWGS criteria. Overall, SARC-F showed the lowest diagnostic accuracy. The Area Under the receiver operating characteristic Curves (AUC) of calf circumference, SARC-F, SARC-CalF, and Ishii's score chart were 0.77 (95% confidence interval [CI], 0.66-0.88), 0.58 (95% CI, 0.42-0.74), 0.75 (95% CI, 0.62-0.87), and 0.78 (95% CI, 0.65-0.90), respectively. The mean AUC of SARC-F was inferior to SARC-CalF (0.58 vs. 0.75, p = 0.035).

The accuracy and diagnostic properties of calf circumference, SARC-CalF, and Ishii's score chart were comparable (mean AUC of 0.77, 0.75, and 0.78, respectively). SARC-F showed the lowest accuracy (mean AUC = 0.58). The recommended screening tools are calf circumference, SARC-CalF, and Ishii's score chart. It is not recommended to rely solely on SARC-F for screening sarcopenia after stroke. We proposed potential new cutoff points for each screening instrument, including SARC-F, SARC-CalF, calf circumference in women, and Ishii's score chart for both men and women.

Macrophages are key innate immune cells in the muscle environment of sarcopenia patients, significantly influencing muscle stem cell (MuSC) proliferation and differentiation. However, prolonged activation of macrophages can hinder muscle recovery. In this study, it synthesizes lipoic acid-modified gold nanoparticles (LA-Au NPs) of varying sizes to evaluate their biocompatibility and immunomodulatory effects. The findings demonstrate that LA-Au NPs exhibit excellent biocompatibility with macrophages and promoted M2 polarization in a size-dependent manner. Mechanistically, LA-Au NPs facilitated metabolic reprogramming in macrophages by enhancing lysosomal autophagy and mitochondrial oxidative phosphorylation. Furthermore, macrophages are shown to chemotax toward MuSCs, regulating their proliferation via the chemokine system, inhibiting MuSC apoptosis, and enhancing differentiation under inflammatory conditions. In vivo studies have confirmed the safety and efficacy of LA-Au NPs in sarcopenia mice. To further enhance the effectiveness of LA-Au NPs, it investigates a delivery strategy that involves preconditioning macrophages with LA-Au NPs (Mac@Au NPs). Compared to the direct injection of LA-Au NPs, Mac@Au NPs demonstrate significantly greater benefits for muscle repair. This highlights the potential of macrophage therapy as a promising strategy for effective muscle regeneration and therapeutic intervention in sarcopenia.

This study aims to investigate the relationship between handgrip strength (HGS) and the progression of chronic kidney disease (CKD) in non-dialysis patients in China, as part of the Self-Management Program for Patients with CKD Cohort (SMP-CKD).

In the SMP-CKD cohort, we utilized Cox regression and Kaplan-Meier survival analysis to explore the association between HGS and CKD progression. Data were stratified by sex-specific HGS quartiles, sarcopenia status, and HGS thresholds. The HGS thresholds were determined through curve analysis of HGS against composite renal outcomes. Group differences were compared to assess the impact of HGS on CKD outcomes.

A total of 441 participants (mean age 57.0 ± 17 years, 56.0% male) with CKD stages 3-5 from the SMP-CKD cohort who underwent grip strength evaluation between April 2019 and June 2024 were included in the analysis. The findings revealed that participants in the highest bilateral HGS quartile had a significantly lower risk of renal endpoints, with a hazard ratio (HR) of 0.102 (95% CI 0.041-0.255) compared to those in the lowest quartile. Patients without sarcopenia had a significantly lower risk of CKD composite outcomes, including increased serum creatinine or acute CKD exacerbations (HR 0.422, 95% CI 0.211-0.844, p < 0.012), as well as severe renal endpoints (HR 0.265, 95% CI 0.101-0.694, p < 0.003). Gender-specific cutoffs identified through log-rank test were 63.7 kg for men and 34.6 kg for women. Participants with bilateral HGS above these thresholds demonstrated better renal outcomes, underscoring the protective effect of higher HGS against CKD progression.

The study provides strong evidence that HGS is a crucial factor in reducing the risk of CKD progression. Higher levels of HGS are significantly associated with a lower occurrence of renal endpoint events.

Undaria pinnatifida fucoidan (UPF), a bioactive sulphated polysaccharide, is widely recognised for its anti-inflammatory, antioxidant, antitumor, anticoagulant, antiviral, and immunomodulatory properties. However, the precise mechanisms by which UPF regulates inflammation and neuronal health remain unclear. This study aimed to investigate the effects of UPF supplementation on pro-inflammatory cytokines in skeletal muscle, small intestine, and the hypothalamus, as well as plasma cytokine levels. Additionally, a brain proteomic investigation in the nucleus accumbens (NAc) was performed to assess UPF's impact on neuronal protein expression in mice. A total of 64 C57BL/6J mice were administered either a standard chow or high-fat diet (HFD) with or without UPF (400 mg/kg/day) for 10 weeks. In HFD-fed mice, UPF significantly reduced the expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in skeletal muscle, small intestine, and hypothalamus, while also lowering circulating IL-1α and IL-6 levels. Proteomic analysis of the NAc revealed that UPF modulated proteins involved in oxidative stress, neuroinflammation, neurotransmitter regulation, and endoplasmic reticulum stress. In contrast, in chow-fed mice, UPF had no effect on the neuroinflammatory-oxidative stress markers but influenced the abundance of proteins associated with immune response and innate immunity. These findings suggest that UPF modulates stress-response pathways in a diet-dependent manner, supporting its potential neuroprotective role in inflammation-related disorders and brain health.

Parkinson's disease (PD) and sarcopenia are prevalent age-related conditions that often coexist in affected individuals. Sarcopenia is particularly common among PD patients, with severe cases affecting approximately one in five individuals with the disease. Furthermore, sarcopenia is closely linked to the accelerated progression of PD, diminished quality of life, greater susceptibility to falls and fractures, and increased mortality risk. Although the precise mechanisms remain unclear, numerous studies suggest that factors such as the accumulation of α-Synuclein in skeletal muscle, loss of motor neurons, inflammation, phosphate toxicity, hormonal dysregulation, vitamin D deficiency, intestinal flora imbalances, and dysfunction of the gut-muscle-brain axis contribute to sarcopenia in PD. Understanding these mechanisms provides valuable insights into the relationship between PD and sarcopenia and establishes a foundation for future research and therapeutic strategies. This review examines the mechanisms underlying sarcopenia in PD, methods for its screening and assessment, and potential avenues for future research, including strategies for risk reduction and treatment.

Muscle wasting and weakness (sarcopenia) are commonly associated with COPD causing frailty and reduced quality of life. The contribution of inflammation to muscle loss and the susceptibility to rapid lung function decline is debated. We hypothesised that comparing the muscle transcriptome to circulating inflammatory cytokine profiles in patients would identify any contribution of systemic inflammation to muscle atrophy.

Quadriceps differential gene expression was determined between mild-COPD (n=28) and severe-COPD (n=51) using GSE100281. These microarray data were compared by biweight mid-correlation with lung function and plasma cytokine levels from the same patients.

Patients with severe COPD had reduced fat-free mass index (a measurement of muscle mass) compared with patients with mild COPD despite similar physical activity and inflammatory cytokine levels. Gene sets associated with inflammation and epithelial mesenchymal transition (EMT) were elevated in severe COPD, suggesting that inflammation may contribute to the loss of muscle mass. In patients with severe COPD, EMT and inflammation gene sets were strongly associated with circulating proinflammatory and anti-inflammatory cytokines. However, in patients with mild COPD, anti-inflammatory cytokines showed negative associations with these gene sets and associations with proinflammatory cytokines were weak. In data from lung and blood samples, patients with severe COPD had elevated inflammatory and EMT gene expression compared with patients with mild COPD suggesting that this phenomenon is not muscle-specific.

In patients at the severe end of the COPD spectrum, the proinflammatory response in muscle predominates, whereas in patients at the mild end of the spectrum, the anti-inflammatory response predominates. This suggestion needs confirming in a longitudinal cohort.

Several studies have suggested that increased intake of saturated fatty acids (SFAs) may have a pro-inflammatory effect, potentially impacting muscle mass and strength. However, the relationship of plasma SFAs and their subtypes (which reflect dietary SFA intake) with muscle mass and strength remains poorly understood. This study aimed to evaluate the association of plasma SFAs with lean mass and handgrip strength in adults.

A cross-sectional study was conducted with 896 participants aged 20-59 years, selected from a subsample of the National Health and Nutrition Examination Survey (NHANES) 2011-2012. Total plasma SFAs and their subtypes were detected using gas chromatography-mass spectrometry. Lean mass was assessed using dual-energy X-ray absorptiometry, with evaluations of both total lean mass and appendicular lean mass. Muscle strength was measured using a handgrip dynamometer, with combined grip strength calculated by summing the highest values from each hand. Linear regression analysis was conducted to examine the association between plasma SFAs, lean mass, and handgrip strength, adjusting for potential confounders.

Total lean mass was negatively associated with total plasma SFAs and several of their subtypes such as plasma levels of stearic acid, palmitic acid, arachidic acid, tricosanoic acid, lignoceric acid, and docosanoic acid. Similarly, appendicular lean mass was negatively associated with total plasma SFAs, as well as with several specific subtypes, including palmitic acid, stearic acid, margaric acid, pentadecanoic acid, and myristic acid. Handgrip strength also demonstrated a negative association with total plasma SFAs, including specific subtypes such as lauric acid, palmitic acid, capric acid, margaric acid, pentadecanoic acid, and myristic acid.

Total plasma SFAs and several of their subtypes are inversely associated with lean mass and muscle strength in adults.

This study aimed to investigate the association between handgrip strength (HGS) and cardiovascular disease (CVD) in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) using data from the UK Biobank cohort.

A total of 201 563 participants were enrolled in this study. The HGS was measured using a Jamar J00105 hydraulic hand dynamometer. MASLD was defined as the presence of hepatic steatosis accompanied by one or more cardiometabolic criteria. Hepatic steatosis was identified using a fatty liver index ≥ 60. Advanced liver fibrosis was defined by a fibrosis-4 (FIB-4) score > 2.67. To examine the differences in the incidence of CVD, male and female participants were divided into non-MASLD, MASLD with high HGS, MASLD with middle HGS, and MASLD with low-HGS groups.

Of the study participants, 75 498 (37.5%) were diagnosed with MASLD, with a mean age of 56.5 years, and 40.6% were male. The median follow-up duration was 13.1 years. The frequency of incident CVD events increased significantly across groups: 10.9% in non-MASLD, 13.3% in MASLD with high HGS, 14.8% in MASLD with middle HGS, and 18.4% in MASLD with low HGS for males (p < 0.001). In females, the frequency of incident CVD events was 6.1% in non-MASLD, 9.2% in MASLD with high HGS, 10.7% in MASLD with middle HGS, and 13.3% in MASLD with low HGS (p < 0.001). Using the non-MASLD group as a reference, multivariate-adjusted hazard ratios (HRs) (95% confidence intervals [CI]) for CVD varied according to HGS in individuals with MASLD. In males with MASLD, HRs (95% CI) were 1.03 (0.96-1.10) for high HGS, 1.14 (1.07-1.21) for middle HGS, and 1.38 (1.30-1.46) for low HGS; in females with MASLD, they were 1.07 (0.97-1.18) for high HGS, 1.25 (1.14-1.37) for middle HGS, and 1.56 (1.43-1.72) for low HGS. The incidence of CVD events increased as HGS decreased in participants with MASLD, regardless of the presence or absence of advanced liver fibrosis (all p < 0.001).

This large prospective cohort study using the UK Biobank showed that in MASLD, a decrease in HGS was associated with increased CVD risk.

This research examines the replicability and generalizability of the association between purpose in life and grip strength. An individual-participant meta-analysis of 27 samples (total N=115,972) from 24 countries that spanned four continents (Asia, Europe, North and South America) with self-reported purpose in life and dynamometer-assessed grip strength. Purpose in life was associated with stronger grip strength in every sample and aggregated in a random-effects meta-analysis (meta-analytic estimate=.06, p<.001). The association was similar across samples from different world regions and not moderated by methodological factors (e.g., scale content). The association was apparent across age, sex, race, and education and slightly stronger among males and participants with relatively less education. Every standard deviation in purpose was associated with a 23% lower likelihood of weak grip strength (meta-analytic OR=.81, 95% CI=.79-.84, p<.001) based on a standard threshold. Purpose in life is associated with grip strength, a marker of overall musculoskeletal health. The association replicates across diverse locations around the world and generalizes across sociodemographic groups.

As society ages, identifying individuals at risk of sarcopenia becomes essential. Several plasma biomarkers are used to assess musculoskeletal status, but their results are inconsistent. Extracellular vesicles (EVs) are investigated as disease biomarkers due to their role in transporting molecules and influencing cellular processes. This study investigated the correlation of known sarcopenia biomarkers-adiponectin, myostatin, P3NP, CRP and TNF-α-measured from plasma-derived EVs with muscle mass, function and performance in an Osteoporosis Sarcopenia cohort at the Seoul National University Bundang Hospital.

Muscle mass was evaluated by measuring appendicular skeletal muscle mass (ASM) using dual X-ray absorptiometry and calculated as ASM/height2. Hand grip strength was measured using a hydraulic hand dynamometer for muscle function and physical performance based on the Short Physical Performance Battery (SPPB), walking speed and the five-time-sit-to-stand test. Density gradient ultracentrifugation was used to isolate EVs from the plasma, followed by confirming the expression of sarcopenia biomarkers. Multivariate regression analysis, adjusted for sex, age, body mass index, smoking, drinking, and bone density, was performed.

The mean age of participants was 74.3 ± 12.1 years (range, 52.0-96.0), with 88.2% being female. Plasma-derived EV levels of myostatin and P3NP were significantly associated with walking speed (ꞵ = -0.309, p = 0.014) and SPPB (ꞵ = -0.276, p = 0.029), respectively. TNF-α levels were strongly correlated with hand grip strength (ꞵ = -0.313, p = 0.013). Using receiver-operating characteristic curve analysis, cutoff values for three factors were determined, allowing participants to be categorized into high and low groups. Low myostatin group had a higher hand grip strength (19.63 kg vs. 17.14 kg, p = 0.027) and faster five-time-sit-to-stand test times (17.34 s vs. 23.72 s, p = 0.032). Low P3NP levels showed a stronger grip strength (19.87 kg vs. 16.81 kg, p = 0.008), better SPPB scores (9.10 vs. 8.03, p = 0.006) and five-time-sit-to-stand times (18.31 s vs. 21.87 s, p = 0.002). Low TNF-α levels were linked to better walking speeds (0.82 m/s vs. 0.64 m/s, p = 0.009) and lower SARC-F scores (1.73 vs. 3.26, p = 0.029).

Our research confirmed that EVs-derived myostatin, P3NP and TNF-α are strongly associated with muscle function and performance. Significant differences in these factors between high and low groups based on biomarker cutoffs emphasize their diagnostic relevance for sarcopenia. These findings offer a promising avenue for identifying effective markers in future research and clinical applications.

Polycystic ovarian syndrome (PCOS) is a prevalent endocrine disorder that causes an inversion of the normal luteinizing hormone (LH) to follicle-stimulating hormone (FSH) ratio. Females with PCOS also experience chronic inflammation. This hormonal imbalance and persistent inflammation can reduce muscle strength and mass. Consequently, this may affect the lumbopelvic muscles, potentially leading to postural abnormalities and spinal misalignment. The study's goals were to find out how the biomechanics of women with PCOS differ from those who did not have the condition and to confirm the link between lumbopelvic parameters and the LH/FSH ratio in women with PCOS. The researcher conducted a case-control study on 95 nulliparous females, with 52 having PCOS and classified as a study group and 43 as a control group. The participants ranged in age from 25 to 35 years, and their body mass index ranged from 25 to 29.9 kg/m2. All participants were selected from the gynecological outpatient clinic of Om El-Masryeen Hospital. The researcher used a pelvic inclinometer to evaluate the pelvic inclination angle and an inclinometer to examine the lumbar angle. Additionally, the researcher simultaneously collected blood samples on the third day of the menstrual cycle. Females with PCOS had significantly higher pelvic inclination and lumbar curve angles than controls (p < 0.05). LH/FSH ratio strongly correlated with lumbar angle and pelvic inclination. Females with PCOS had greater pelvic tilting and exaggerated lumbar lordosis than controls. The LH/FSH ratio showed a strong correlation with both the lumbar curve angle and pelvic inclination in PCOS.Clinical trial: The clinical trial number [NCT03740932] with initial release date at 09/17/2024.

Sarcopenia has known negative effects on clinical and oncological outcomes in patients with colorectal cancer (CRC). The use of the Strength, Assistance in walking, Rise from a chair, Climb stairs, and Falls (SARC-F) questionnaire to determine the effects of sarcopenia on postoperative complications of CRC has not been reported to date. Therefore, this study aimed to investigate the relationship of SARC-F score with clinicopathologic outcomes after CRC surgery.

We retrospectively included 285 patients who completed SARC-F questionnaires before CRC surgery between July 2019 and March 2022. Patients with an SARC-F score ≥4 (total score: 10) were classified in the high SARC-F group.

Overall, 34 (11.9%) patients had high SARC-F scores. These patients were older (76.9 ± 8.5 vs. 64.5 ± 11.4 years, p < 0.001) and had a higher preoperative CRP (2.5 ± 3.9 vs. 0.8 ± 1.6 mg/L, p = 0.019), lower body mass index (21.7 ± 3.4 vs. 24.0 ± 3.8 kg/m2, p = 0.001), and higher pan-immune-inflammation value (632.3 ± 615.5 vs. 388.9 ± 413.8, p = 0.031). More postoperative complications were noted in the high SARC-F group than in the low SARC-F group (58.8% vs. 35.6%, p = 0.009). High SARC-F scores were significantly associated with higher nodal stage, higher number of harvested lymph nodes, and larger tumor size. Univariate and multivariate analyses revealed high SARC-F score and operation time as independent risk factors associated with postoperative complications (odds ratio, 2.212/1.922; 95% confidence interval, 1.021-4.792/1.163-3.175; p = 0.044/0.011, respectively).

Preoperative SARC-F score was an independent risk factor associated with postoperative complications following colorectal cancer surgery.

The association between changes in physical functions and stroke incidence remains uncertain.

A total of 7978 participants without stroke from the China Health and Retirement Longitudinal Study (CHARLS) were recruited in 2011-2012 and followed up until 2020. We assessed annual changes in physical functions from 2011 to 2015, including absolute grip strength, relative grip strength, walking speed, chair-rising time and standing balance. The Cox proportional hazards model was applied to assess the longitudinal associations between annual changes in physical functions and stroke. Restricted cubic spline analyses were used to explore the dose-response relationships.

During 71 714 person-years of follow-up, 549 incident stroke cases were reported. For each 1-kg absolute grip strength increment, 0.1-unit relative grip strength increment, or 1-point standing balance test score increment, the hazard of stroke was reduced by 12% [hazard ratio (HR): 0.88; 95% confidence interval (CI): 0.84-0.93], 53% (HR: 0.47; 95% CI: 0.34-0.64), 55% (HR: 0.45; 95% CI: 0.30-0.67), respectively. We found a negative linear dose-response association of the annual change in absolute and relative grip strength with incident stroke, as well as a nonlinear association between the annual change in standing balance and incident stroke. However, neither the annual change in walking speed nor chair-rising time was related to the incident stroke.

A greater improvement in absolute grip strength, relative grip strength or standing balance was suggested to be associated with a lower risk of stroke amongst middle-aged and older people. These objectively measured physical function changes are imperative for high-risk population classification and stroke prevention.

Sarcopenia, a chronic degenerative condition associated with aging, is characterized by a significant decline in muscle mass and strength. Puerarin, a major active isoflavone extracted from Pueraria lobata, exhibits potent anti-inflammatory and antioxidant properties. However, its therapeutic effects on sarcopenia remain unclear. Thus, the purpose of this study was to evaluate the therapeutic effects and underlying molecular mechanisms of puerarin in ameliorating sarcopenia in naturally aged mice. Twenty-month-old male C57BL/6 J aged mice were randomly divided into two groups based on body weight: the puerarin group (puerarin dissolved in double-distilled water, 150 mg/kg/day) and the control group (equal volume of double-distilled water). After an 8-week intervention, changes in muscle mass and function between the two groups were compared. Techniques such as HE staining, immunofluorescence staining, ELISA, transmission electron microscopy, Western blot, and qRT-PCR were employed to evaluate the positive effects of puerarin on sarcopenia in naturally aged mice. Furthermore, serum proteomics and muscle transcriptomics were used to analyze the molecular mechanisms underlying the anti-muscle atrophy effects of puerarin. The results demonstrated that puerarin significantly improved body composition, enhanced muscle mass and function, and exerted its effects by modulating inflammatory cytokines, reducing oxidative stress, and inhibiting the expression of apoptosis proteins in skeletal muscle. Additionally, integrated proteomics and transcriptomics analyses suggested that the anti-muscle atrophy mechanisms of puerarin might be related to the TNF-α/NF-κB signaling pathway. These findings highlight puerarin's potential as a therapeutic agent for sarcopenia, providing a foundation for further research and clinical application.

Adipogenesis is intricately linked to the onset and progression of muscle aging; however, the relevant biomarkers remain unclear. This study sought to identify key genes associated with adipogenesis in the context of muscle aging. Firstly, gene expression profiles from biopsies of the vastus lateralis muscle in both young and elderly population were retrieved from the GEO database. After intersecting with the results of differential gene analysis, weighted gene co-expression network analysis, and sets of adipogenesis-related genes, 29 adipogenesis-related differential expressed genes (ARDEGs) were selected. Connectivity Map (cMAP) analysis identified tamsulosin, fraxidin, and alaproclate as key target compounds. In further, using three machine learning algorithms and the friends analysis, four hub ARDEGs, ESRRA, RXRG, GADD45A, and CEBPB were identified and verified in vivo aged mice muscles. Immune infiltration analysis showed a strong link between several immune cells and hub ARDEGs. In all, these findings suggested that ESRRA, RXRG, GADD45A, and CEBPB could serve as adipogenesis related biomarkers in muscle aging.

ObjectivesThis study investigated the associations between Five-Factor Model personality traits and balance impairment and lower limb strength.MethodsMiddle-aged and older adults (Age range: 34-104 years; N >27,000) from six large samples from the US and England were assessed for standing balance, lower limb strength, personality traits, sociodemographic, and health-related variables.ResultsHigher extraversion, openness, agreeableness, and conscientiousness were related to lower balance impairment risk and better lower limb strength. Higher neuroticism was associated with higher risk of balance impairment and with weaker lower limb strength. Biological, clinical, behavioral, and psychological factors partially accounted for these associations between personality and risk of balance impairment. Depressive symptoms and physical activity partially mediated the associations between personality traits and limb strength.DiscussionPersonality traits have replicable associations with lower extremity functions. The study identifies potential moderators and mediators of these associations.

Redox signaling acts as a critical mediator in the dynamic interactions between organisms and their external environment, profoundly influencing both the onset and progression of various diseases. Under physiological conditions, oxidative free radicals generated by the mitochondrial oxidative respiratory chain, endoplasmic reticulum, and NADPH oxidases can be effectively neutralized by NRF2-mediated antioxidant responses. These responses elevate the synthesis of superoxide dismutase (SOD), catalase, as well as key molecules like nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), thereby maintaining cellular redox homeostasis. Disruption of this finely tuned equilibrium is closely linked to the pathogenesis of a wide range of diseases. Recent advances have broadened our understanding of the molecular mechanisms underpinning this dysregulation, highlighting the pivotal roles of genomic instability, epigenetic modifications, protein degradation, and metabolic reprogramming. These findings provide a foundation for exploring redox regulation as a mechanistic basis for improving therapeutic strategies. While antioxidant-based therapies have shown early promise in conditions where oxidative stress plays a primary pathological role, their efficacy in diseases characterized by complex, multifactorial etiologies remains controversial. A deeper, context-specific understanding of redox signaling, particularly the roles of redox-sensitive proteins, is critical for designing targeted therapies aimed at re-establishing redox balance. Emerging small molecule inhibitors that target specific cysteine residues in redox-sensitive proteins have demonstrated promising preclinical outcomes, setting the stage for forthcoming clinical trials. In this review, we summarize our current understanding of the intricate relationship between oxidative stress and disease pathogenesis and also discuss how these insights can be leveraged to optimize therapeutic strategies in clinical practice.

This study aims to explore the combined risk of metabolic syndrome (MetS) and low fat-free mass (FFM) on an individual's disability-free survival (DFS). Disability is defined as a composite of dementia, physical disability, and mortality.

Using data from the Korean Genome and Epidemiology Study, we divided 3721 participants aged 40-69 years based on their MetS status and FFM index (FFMI) score. Kaplan-Meier survival analysis and Cox regression were used to analyze differences in DFS between the four groups.

From 108 events, MetS group had significantly shorter DFS than the non-MetS group regardless of FFMI (p < 0.0001). After adjusting other potential confounding variables, the MetS group had a higher risk of shortened DFS regardless of FFMI, and the MetS group with low FFMI had a 2.06-fold increased risk compared to the non-MetS group with high FFMI (p < 0.001). Older age and lower income were also associated with higher risk of shorter DFS (p < 0.001).

The combination of MetS and low FFMI contribute to a cumulative risk of shortened DFS. Community nurses can perform MetS screening and body composition assessment to predict and control the risk of developing disability over time.

Acute inflammatory diseases require suitable medicine over the existing therapeutics. In this line, the present work is focused on developing polymeric nanomedicine for the treatment of inflammatory disorders. Herein, cell viable nanoparticles (GlyNPs) of size 180-250 nm in diameter and pore size of 4-5 nm in diameter, based on glycine and acryloyl chloride, have been developed and proved to be a potential anti-inflammatory agent without using any conventional drugs. These particles exhibit colloidal stability (with a zeta potential of -35.6 mV). A network pharmacology-based computational study has been executed on 9076 genes and proteins responsible for inflammatory diseases, out of which 10 are selected that have a major role in rheumatoid arthritis (RA). In silico docking study has been conducted to find out the targeted efficiency of the GlyNPs considering 10 inflammation-specific markers, namely IL-6, IL-1β, TNF-α, TLR-4, STAT-1, MAPK-8, MAPK-14, iNOS, NF-κβ and COX-2. The results revealed that the GlyNPs could be an excellent anti-inflammatory component similar to aspirin. The in vitro inflammation activity of these GlyNPs has also been checked on an inflammation model generated by LPS in RAW 264.7 macrophages. Then, the in vitro anti-inflammation efficiency has been checked with 10-150 μg mL-1 of GlyNP doses. The treatment efficiency has been checked on inflammation-responsible immune markers (NO level, NF-κβ, INF-γ, IL-6, IL-10, and TNF-α) and it was found that the GlyNPs are an excellent component in reducing inflammation. The in vivo therapeutic response of GlyNPs on the induced rheumatoid arthritis (RA) model has been evaluated by measuring the morphological, biochemical and immune-cytokine and interferon levels responsible for the inflammation, using a 2 g kg-1 dose (sample to weight of rat). The anti-inflammatory efficiency of GlyNPs without using additional drugs was found to be excellent. Thus, GlyNPs could be paramount for the potential treatment of various inflammatory diseases.

Vitamin D insufficiency has been frequent in women with breast cancer (BC), as well as impaired muscle strength (MS), and a possible relationship between these conditions has been investigated in different populations, except in women with BC. This study aimed to analyze the association between serum vitamin D levels and MS in women with BC. Observational cross-sectional study carried out with adult women with BC, without metastasis/recurrence, with up to 12 months of diagnosis. Serum 25(OH)D concentration was categorized as insufficient (<30 ng/mL) or sufficient (≥30 ng/mL). MS was assessed by the Handgrip Strength test and divided into strength tertiles of the population itself: 1st tertile (6-21 kg), 2nd tertile (22-26 kg), and 3rd tertile (27-39 kg). Adjusted multinomial logistic regression models verified the association of serum vitamin D levels in MS tertiles, with a significance of 5%. A total of 151 women were evaluated. Most women had insufficient levels of vitamin D (70%). Insufficient serum vitamin D levels were associated with the 1st and 2nd tertile of MS (odds ratio [OR]: 5.74, 95% confidence interval [CI]: 1.77-18.64, P = 0.004; OR: 4.48, 95% CI: 1.34-14.97, P = 0.015, respectively). Serum vitamin D insufficiency incresed the probability to present lower tertiles of MS in women with BC.

Sarcopenia is a common indicator of systemic nutritional status in patients with cancer progression. This study investigated the impacts of sarcopenia on adverse effects and prognosis of sarcopenia on patients with esophageal cancer receiving chemoradiotherapy.

The clinical data of 158 patients with initially diagnosed esophageal cancer who received chemoradiotherapy were collected, and nutritional indexes and inflammatory markers were calculated. The cross-sectional areas of the skeletal muscle, subcutaneous fat and visceral fat were calculated using computed tomography (CT) images of the midpoint of the third lumbar (L3) vertebra. The incidence of adverse events, response evaluation, 1-year and 3-year overall survival (OS) and progression-free survival (PFS) were compared between sarcopenia group and non-sarcopenia groups.

This study included 158 patients, 103 (71.5%) in the sarcopenia group and 45 (28.5%) in the non-sarcopenia group. The last follow-up date was January 31, 2024. The median follow-up time was 36 months for all patients. The chi-square test revealed no significant difference in the incidence of serious adverse events between the two groups. The complete response rates (CR) of patients in the sarcopenia and non-sarcopenia groups 1 month after chemoradiotherapy were 2.7 and 13.3%, respectively, p = 0.017, and the difference was statistically significant. Moreover, the objective response rates (ORR) were 38.9 and 60.0%, respectively (χ2 = 5.770, p = 0.016). The median survival time for all patients was 36 months [95% Confidence Interval CI 24-48]. Univariate analysis (Cox proportional risk model) showed that sarcopenia, KPS score, albumin level, T stage, and N stage were correlated with patients' OS. Multivariate analysis showed that sarcopenia (Hazard Ratio HR 2.84, 95%CI [1.45-5.57], p = 0.002), KPS score, albumin level and N stage were independent prognostic factors for OS.

Sarcopenia reduced OS in patients with EC treated with chemoradiotherapy. It can be used as an independent indicator to predict the OS of such patients, which may help in developing optimal treatment strategies.

In previous studies, several inflammatory biomarkers derived from complete blood cell counts (CBC), such as systemic immune inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), and non‑high‑density lipoprotein cholesterol to high‑density lipoprotein cholesterol ratio (NHHR) have been identified as predictors of sarcopenia. However, whether Monocyte to High-Density Lipoprotein Cholesterol Ratio (MHR) can predict the development of sarcopenia has not yet been established. The research first attempts to investigate the association between MHR and low muscle mass and to compare the predictive abilities of MHR, SII, NLR, and NHHR for low muscle mass risk.

The study comprised 10,321 participants aged 20 years and above from the United States. Multiple logistic regression was performed to explore the association between ln-transformed MHR, SII, NLR, NHHR and low muscle mass. Additionally, AUC values and ROC curves were used to assess the predictive effectiveness of ln MHR and other markers (ln SII, ln NLR, ln NHHR, ln MHR + ln SII, ln MHR + ln NHHR, and ln MHR + ln NLR). The bootstrap estimated 95% Cl was shown with the AUC.

In the fully adjusted model, ln SII, ln NLR, ln NHHR, ln MHR, ln MHR + ln SII, ln MHR + ln NHHR, and ln MHR + ln NLR were positively associated with low muscle mass (ln SII: OR = 1.59 [1.37-1.84]; ln NLR: OR = 1.35 [1.13-1.60]; ln NHHR: OR = 1.49[1.27-1.75]; ln MHR: OR = 1.98 [1.68-2.33]; ln MHR + ln SII: OR = 1.61 [1.46-1.79]; ln MHR + ln NHHR: OR = 1.42 [1.29-1.56]; ln MHR + ln NLR: OR = 1.58 [1.41-1.78]). Compared to the lowest quartile of ln MHR, higher quartiles were significantly associated with increased odds of low muscle mass (P for trend < 0.0001). In ROC analysis, ln MHR + ln SII had a higher AUC value than other indicators (AUC = 0.608).

Ln-transformed MHR, SII, NLR, and NHHR were positively associated with low muscle mass. MHR outperforms SII, NLR, and NHHR in predicting sarcopenia.

Muscle quality index (MQI), an emerging health index, is calculated by dividing handgrip strength by skeletal muscle mass. Current evidence on the correlation between MQI and type 2 diabetes mellitus (T2DM), insulin resistance (IR) is limited. This work aims to study that correlation.

This study involves a cross-sectional analysis on data from the National Health and Nutrition Examination Survey (NHANES) during the period from 2011 to 2014. To explore the correlation between MQI, IR and T2DM, multivariate logistic regression, receiver operating characteristic (ROC) curve, subgroup analysis, and restricted cubic spline regression were employed.

A total of 2816 American adults were enrolled in this study, among whom 1264 (44.9%) had IR, and 300 (10.7%) had T2DM. Logistic regression and RCS regression analyses showed a significant negative linearly correlation between MQI and the prevalence of IR (OR = 0.708, 95%=0.514, 0.976) and T2DM (OR = 0.676, 95%CI = 0.472, 0.969). Subgroup analysis further revealed a stronger correlation between MQI and IR among individuals with obesity. ROC analysis showed that compared with skeletal muscle and grip strength, MQI (AUC = 0.679 for IR and 0.688 for T2DM) can serve as a more reliable identification factor for IR and T2DM.

This study provides evidence that decreased levels of MQI are correlated with an increased risk of IR and T2DM, indicating the potential utility as a marker for identifying IR and T2DM.

With the exacerbation of global population aging, sarcopenia has become an increasingly recognized public health issue. Sarcopenia, characterized by a progressive decline in skeletal muscle mass, strength, and function, significantly impacts the quality of life in the elderly. Herein, we explore the role of chroniclow-gradeinflammation in the development of sarcopenia and its underlying molecular mechanisms, including chronic inflammation-associated signaling pathways, immunosenescence, obesity and lipid infiltration, gut microbiota dysbiosis and intestinal barrier disruption, and the decline of satellite cells. The interplay and interaction of these molecular mechanisms provide new perspectives on the complexity of the pathogenesis of sarcopenia and offer a theoretical foundation for the development of future therapeutic strategies.

Chronic kidney disease (CKD) is a progressive condition linked to sarcopenia, a syndrome characterized by loss of skeletal muscle mass and strength, affecting a quarter of CKD patients globally. Sarcopenia has multiple paths through which it can worsen morbidity and mortality as well as decrease the quality of life in CKD, including systemic inflammation, hormonal imbalances, metabolic changes, and dysbiosis of gut microbiota. There is a regional variation in the criteria set for diagnosis, with two main groups being the European Working Group on Sarcopenia in Older People and the Asian Working Group for Sarcopenia. Management regimes such as nutritional optimization, vitamin D, exercise, correction of metabolic acidosis, and modulation of gut microbiota constitute effective intervention strategies. Emerging therapeutic options include anabolic agents, myostatin inhibitors, and anti-inflammatory treatment options. Future advances such as genomics, proteomics, and personalized medicine will open up new avenues for addressing the complex pathophysiology of sarcopenia. Hence, a comprehensive multidisciplinary approach focused on the specific needs of each patient will be vital in reducing the effects of sarcopenia and improving the situation of people with CKD.

The European Working Group on Sarcopenia in Older People (EWGSOP2) defines sarcopenia as a muscle disease (muscle failure) rooted in adverse muscle changes that accrue across a lifetime; sarcopenia is common among adults of older age. New findings on the hormonal and metabolic characteristics of patients with sarcopenia have aided in developing more targeted therapeutic strategies. However, treating older patients with sarcopenia still poses a number of challenges. Despite numerous studies on sarcopenia, no comprehensive phenotyping of older sarcopenic patients has yet to be offered. Cluster analysis has been successfully used to study various diseases. It may be extremely advantageous for collecting data on specific sarcopenia progressions based on a simultaneous assessment of a whole range of factors.

To identify disease progression specific to older patients based on cluster analysis of blood biomarkers and lifestyle.

 This study included 1709 participants aged 90 and older. The median age was 92. Seventy-one percent of participants were female. Participants underwent a comprehensive geriatric assessment and had their metabolic, hormonal, and inflammatory blood biomarkers measured. The data were analyzed and clustered using the R programming language.

 Seven sarcopenia clusters were identified. The most significant variables, in descending order, were malnutrition, physical activity, body mass index, handgrip strength, testosterone, albumin, sex, adiponectin, total protein, vitamin D, hemoglobin, estradiol, C-reactive protein, glucose, monocytes, and insulin. Handgrip strength measurements and free T3 levels increased linearly between the cluster with the lowest measurements and the cluster with the highest measurements.

The findings of this study may greatly aid in understanding the relationship between blood biomarkers, lifestyle and sarcopenia progression in older adults, and may help in developing better prevention and diagnostic strategies as well as more personalized therapeutic interventions.